To what extent do researchers agree on the causes and remediation of developmental dyslexia? How do you think any differences should be resolved?

Developmental dyslexia is a specific learning difficulty that primarily affects the acquisition of word reading (and spelling). During early schooling, individuals may display difficulty in acquiring adequate reading skills, reading more slowly or less accurately than expected. The following description of the subject of an early case study of dyslexia captures the challenging paradox faced by the wide variety of researchers of this developmental disorder. “He has always been a bright and intelligent boy…in no way inferior to others of his age. His great difficulty has been…his inability to learn to read….” (Morgan, 1986, cited in Brown, 2003). Why is it that these articulate, intelligent people show such a problem in what seems like one of our most routine skills? Due to this unexpectedness in reading failure and its high incidence in Western populations (between 5% and 15%), dyslexia research has instigated great passion and controversy. Early pioneers in dyslexia research, Morgan, Hinshelwood, and Orton believed that visual problems underlay an apparent ‘wordblindness’. Orton (1925) introduced the term ‘strephosymbolia’ to specify that, although the problem was believed to be primarily visual, it was not one of blindness as such, but one of ‘twisted symbols’, a difficulty in distinguishing the order of letters. However, around a quarter of a century ago, there was a gradual realisation that problems of language must be, at least in part, responsible for the reading deficits (Vellutino, 1979). This general hypothesis has been refined over the years to provide what is arguably the consensus theoretical belief of most dyslexia researchers, namely that dyslexic children suffer from an early impairment in their phonological skills, and this impairment prevents them from acquiring the word decoding and blending skills that are essential for the acquisition of skilled reading. Following on from this consensus, systematic phonics instruction, as a remediation for dyslexia has become largely popular. In addition to this consensus concerning the causes and remediation of developmental dyslexia, this essay will also discuss more recent paradoxical research which highlights how despite this large consensus, there are disagreements among theoreticians over the exact neurological and cognitive basis of the disorder.

Causes of developmental dyslexia

Dyslexia researchers, especially those with a background in psychology have focused on cognitive analyses of the disorder in order to determine the direct cause of the learning failure. A consensus has emerged among the majority of these researchers that the specific reading retardation characteristic of dyslexia is directly and exclusively caused by a cognitive deficit that is specific to the representation and processing of speech sounds: this is the phonological theory of dyslexia or the phonological deficit hypothesis. In line with this view is recent reading-related research that has placed a strong emphasis on understanding the acquisition of reading skill as building upon already developed representations of spoken language (De Gelder & Morais, 1995). Furthermore, ample evidence suggests various phonological variables, especially the ability to consciously manipulate sound units smaller than the whole world (e.g. in the size of phonemes and syllables), labelled phonological awareness, are good predictors of future reading ability and are already poor in would be dyslexics (Pennington & Lefty, 2001). Indeed, there is strong evidence showing that, in addition to the more obvious reading and writing problems, diagnosed dyslexic individuals do display impairments in tasks that involve phonological processing (Snowling, 2000).

For example the metaphonological deficit of phonological awareness, specifically phonemic awareness has been measured in dyslexics using tasks such as phoneme elision. This involves the repetition of a heard word while omitting the first or last sound of that word, for example “cat” without the first sound becomes “at” (McDougall, Hulme, Ellis & Monk, 1994). Dyslexics consistently perform with great difficulty on such tasks, therefore displaying an impairment in the ability to segment words into the single speech sounds. Other phonological processing skills that are frequently shown to be impaired in dyslexics are rapid naming and poor verbal short-term memory. The lack of phonological skills affects the reading of dyslexics through its interaction with the demands of learning to read an alphabetic writing system such as English. Normal reading development of such a system requires the acquisition of phonemic awareness “…if children are to abstract how written words relate to spoken words, and to develop the alphabetic principle” (Snowling, 2000, p.54), the idea that written units (graphemes) can be mapped onto a small set of elements (phonemes) of a language.

A deeper understanding of dyslexia and its’ deficits in phonology has been provided by the medical perspective. As emphasised by Morton and Frith (1995), in trying to understand a developmental disorder such as dyslexia, links between biological and cognitive levels of explanation are needed. Observable behaviour can be explained by a cognitive dysfunction: the cognitive dysfunction can be explained by a (genetic) brain dysfunction. Indeed since its familial aggregation, suggesting a genetic basis, was identified, large scale twin and familial studies (e.g., Smith, Kimberling, Pennington & Lubs, 1983) have established specific abnormalities both of chromosome 15 and, more recently, chromosome ...

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So, at the level of the brain, the cognitive deficit in the phonological system of dyslexia can be seen to arise from a congenital dysfunction of certain cortical areas involved in phonological decoding and reading comprehension. Evidence of this is provided by Galaburda and his colleagues (Galaburda, 1994; Galaburda & Kemper, 1978) who were also interested in the biological substrates of the disorder. Microscopic examinations throughout the perisylvian region of the left hemisphere of dyslexic brains, presented intriguing abnormalities in the form of scarred neurons. Furthermore, it was found that the dyslexic individual’s planum temporale, a part of the Wernicke’s area, were abnormally symmetrical. Since it is well established that the left hemisphere, particularly, the Wernicke’s area, subserve language processing, it is reasonable to infer that the dysfunction of these regions is the origin of what many have now labelled as a core phonological deficit (Snowling, 2000).

Although a deficit in phonological processing as a cause of developmental dyslexia has a wide consensus among researchers and remains the most consistent finding in all psychological studies of dyslexia, the basis of the deficit remains less clear. Largely attributable to an increasingly significant proportion of dyslexics presenting sensory deficits, which the phonological deficit hypothesis is unable to account for, an increasing group of researchers have deviated from this approach and focused on a magnocellular account of dyslexia. This holds that the reading problems derive from impaired sensory processing, caused by abnormal auditory and/or visual magnocellular pathways.

Tallal, Miller and Fitch (1993) for example, are a subset of such researchers who agree with the idea of a phonological deficit but see it as secondary to a more basic auditory impairment. This proposal derived from early studies (Tallal, 1980), which identified impairments in reproducing the order of rapidly presented temporal events. Specifically “a deficit in auditory processing of rapid auditory sounds that are entering the nervous system in the 10’s of millisecond are thought to impact language and subsequently reading because phonemes differ only in frequency changes that in the first 40-50 ms of the sound”(Temple, 2003, p.1). Without this ability to detect rapid auditory signals the child presents problems in phonological discrimination, and thus to reduced phonological skills. These researchers have now linked these problems to underlying abnormalities in the auditory magnocellular system.

Similarly, a related group of researchers maintain that there is an abnormality in the visual magnocellular system of dyslexics. The re-establishment of visual deficits in dyslexia has arisen due to several studies that have reported dyslexics exhibiting impairments in visual processing that are functions of the dorsal visual pathway, a system dominated by magnocellular cells in the lateral geniculate nucleus and is involved in the detection of transient visual information. For instance, Lovegrove and his colleagues (1990) demonstrated that developmental dyslexics had slightly reduced contrast sensitivity at the low spatial frequencies and low luminance levels favoured by the magnocellular system, particularly during flicker. Stein and Walsh (1997), also committed proponents of the visual magnocellular hypothesis and has argued that dyslexic individuals have difficulties with binocular vision. Eden, Vanmeter, Rumsey, Maisog, Woods and Zeffiro (1996) reported a brain-imaging study in which a small sample of dyslexics showed impairments in judging the relative velocity of movement of visual stimuli. In addition they also exhibited abnormal activation in area V5/MT, part of the magnocellular system (Rayner, Foorman, Perfetti, Pesetsky & Seidenberg, 2001).

It should be emphasised that these supporters of the magnocellular theory do not dispute the phonological deficit hypothesis. Rather, they challenge that phonological problems are caused by a basic deficiency in hearing sounds, and that a visual deficit might independently contribute to reading problems. Therefore, on the basis of the two alternative approaches discussed so far: the phonological deficit and magnocellular deficit, it can be seen that dyslexia researchers agree that a phonological deficit is a cause of developmental dyslexia. However differences in the exact degree of centrality of the phonological deficit in explaining the reading retardation and about the importance of apparent sensory impairments in the dyslexic population reduce the strength of the consensus and give rise to an alternative magnocellular account of dyslexia.

Recently, Roderick Nicolson and his colleagues have criticised that “in spite of extensive research, these approaches have failed to account for the full range of difficulties established for dyslexic children” (Nicolson, Fawcett, Dean, 2001, p.508), specifically the more recently established impairments in balance and motor skills. Initial cognitive level arguments (Nicolson & Fawcett, 1990) emphasised an all-encompassing difficulty in skill automatisation, an inability to become completely fluent in cognitive and motor skills to the extent that they no longer need conscious control. The same researchers have now implicated abnormal function of the cerebellum, a system long known to be responsible for motor skill execution and more recently thought to play a central role in skill automatisation and skills relating to language.

Following this, Nicolson et al (2001) claim to account for the full range of difficulties established for dyslexic children in their cerebellar deficit hypothesis. Cerebellar abnormality at birth is hypothesised to lead to problems in skill (motor and articulation), fluency and automaticity. More specifically, the lack of articulatory fluency is seen to lead to impoverished representation of the phonological characteristics of speech, which in turn may lead directly to impaired sensitivity to onset, rime and the phonemic structure of language – that is a deficit in phonological awareness, which leads to the subsequent problems in learning to read. Cerebellar impairment therefore causes by direct means the phonological core deficit. Again at a cognitive level of explanation, proponents of the cerebellar deficit account of dyslexia agree with the vast majority of researchers that a phonological core deficit is a “…fruitful explanatory framework for many aspects of dyslexia…” (Nicolson et al, 2001, p.510), but disagree that it is the sole cognitive dysfunction and also highlight an automatisation deficit. In relation to the theoretical formulation for dyslexia based on a magnocellular deficit, the cerebellar deficit also highlights an underlying neural substrate but is an alternative mechanism to the magnocellular abnormality and addresses a general motor deficit as opposed to a sensory impairment.

Remediation of dyslexia

Regarding the remediation of developmental dyslexia, proposed interventions have been largely based on these theoretical approaches and have therefore varied along with the specific claims concerning the mechanisms responsible for the disorder. However the general agreement among researchers that a lack of phonological skills does somehow or the other play a causal role in dyslexia, transfers to the issue of remediation, specifically that this insufficiency should be addressed, directly or indirectly, in all interventions designed to overcome the disorder. The vast majority of researchers solely in support of the phonological deficit hypothesis, exclusively advocate direct training in aspects of phonology. Systematic phonics instruction, for example has successfully been implemented and teaches the dyslexic the major grapheme-phoneme correspondences and how to use these to decode and spell words. Also it teaches phonemic awareness which is as noted before the ability to analyse and manipulate phonemes in speech, for example, how to break the spoken word ‘beach’ into three phonemes, /b/-/e/-/ch/, or how to blend these phonemes to say the whole word. Acquiring a reasonable grasp of phonics, the dyslexic reader is in a better position to make progress because he or she will be better equipped to identify words encountered in print for the first time (Snowling, 2000).

Although there is widespread use of phonics instruction that has led to direct benefits in helping to overcome dyslexia, the researchers who have recently highlighted the theoretical paradox in dyslexia disagree that phonology should be the primary target of remediation,. Instead they have developed interventions specifically to remediate the sensory and motor impairments in dyslexia. In remediating these difficulties phonology is also seen to improve.

For example, based on her discovery that many children with specific language impairment show a significantly impaired ability to sequence auditory tones presented close together, a difficulty attributed to the auditory magnocellular system, Tallal and her colleagues have developed the ‘Fast ForWord’ remediation training programme (Tallal, Mezenich, Miller & Jenkins, 1998). To overcome this specific difficulty, the programme’s primary focus is on training the children to discriminate rapid auditory signals. Speech, with artificially slowed consonant transition is presented, the idea being that it is possible for the brain to be retrained to become sensitive to the transition. Although the primary focus of the training programme is elsewhere, it too emphasises training in phonological processing. Regarding an abnormality in the visual magnocellular system, proposals for remediation have included wearing coloured glasses or an eye patch. More specifically, Stein, Richardson and Fowler (2000) advocated treatment of difficulties with binocular vision via the occlusion technique.

Similarly, following the cerebellar deficit hypothesis of dyslexia (Nicolson, Fawcett & Dean, 2001), Dore and Rutherford (2001) have proposed that given the plasticity of the cerebellum throughout childhood, it should be possible to retrain the dyslexic cerebellum, leading to more normal functioning, such that learning is scaffolded much more efficiently. They have since developed a systematic Balance Remediation Training Programme, DDAT, based on longstanding principles of balance. Key elements of the exercise treatment include the use of a balance board, throwing and catching of bean bags (including throwing from hand to hand with careful tracking of the eye), and the practice of dual tasking. In a recent evaluation of this DDAT exercise-based treatment for children with reading difficulties, it was concluded that, in addition to its direct effects on balance, dexterity and eye movement control, the benefits of treatment extended to the cognitive skills underlying literacy and the reading process (Reynolds , Nicolson & Hambly, 2003).

In conclusion it can be concluded that, to a large extent researchers agree that a phonological deficit, and the phonics instruction that follows, is the cause and the most beneficial form of remediation, respectively. This is reflected in the predominance of the phonology in dyslexia research and practice for the past 20 years. However a rival area of dyslexia research has challenged this consensus. Although these researchers do agree on the existence of a phonological deficit in dyslexia, their primary focus on sensory and motor impairments in dyslexia has generated very different hypotheses to that of the phonological deficit hypothesis. The lurking question is that of whether they are all correct and co-existable. It is presently argued that the differences between dyslexia researchers need to be resolved as a better understanding of the causes and remediation of dyslexia is likely to lead to the development of better diagnostic procedures, early detection, and successful conquering of the disorder. Resolution could be achieved, perhaps through further research into the possibility of subtypes of developmental dyslexia. The hitherto research in this domain has distinguished between two subtypes, phonological dyslexia and surface dyslexia, where on the basis of the two-route model of reading development, there is damage to the phonological (spelling-to-sound) route, and the visual (whole word) route respectively (Manis, Seidenberg, Doi, McBride-Chang & Petersen, 1995). It could be then that different dyslexic research, especially concerning phonological, auditory and visual impairments, is studying different types of dyslexics. However more extensive research does need to be carried out regarding the issue of subtypes and the underlying causes of dyslexia.

The occurrence of sensory and/or motor disorders more often in the dyslexic than in the non-dyslexic population gives rise to the possibility that dyslexia could be viewed as a general sensorimotor syndrome, as opposed to a specific phonological deficit on the other side of an antagonistic divide. However the prevalence is limited in comparison to that of a deficit in phonological processing. Indeed a recent large scale study (Ramus, Rosen, Dakin, Day, Castellote, White, & Frith, 2003), has found every single dyslexic in their sample to display a phonological deficit, with a third of them seeming to be spared by any concurrent sensory or motor deficit. Another caveat of the proposed sensory and motor disorders is that they seem to have limited consequences on reading skill. The relationship of visual deficits to reading retardation, for example, is hotly debated, especially as visual disorders are frequently accompanied by a phonological deficit. The visual, along with the rest of the sensory and motor hypotheses outlined above are very controversial and overall very different to the largely held phonological deficit. It is therefore unlikely that they will all be able to peacefully co-exist. But until one side of the antagonistic divide decides to give in or are proved wrong it doesn’t seem like their will be any long-term resolution. In the meantime based on this current knowledge, Franck Ramus (2003) proposes a viable immediate resolution, that is the characterisation of dyslexia as a specific phonological deficit, optionally accompanied by a sensorimotor syndrome. Consequently whether or not the remediaition of the dyslexic individual will involve additional or alternative interventions to the successful phonics instruction, will depend on the absence or presence of this optional feature.

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